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184
Abdominal Compartment Syndrome
Table 1. Characteristics of burn patients with IAH or ACS
Series # Pts TBSA Burn Inhalation IAP Early Late
Greenhalgh case series
Greenhalgh prospective
5
Ivy
9
Latenser
8
Hobson
7
Corcos
6
Ivy
10
Tsoutsos
# pts: number of patients in series that developed IAH and or ACS; TBSA Burn: mean percentage of total
body surface area burned in patients with IAH or ACS; Inhalation: presence of inhalation injury; IAP:
mean IAP; Early: development of IAH or ACS within 72 hours of burn injury; Late: development of IAH
or ACS during sepsis episode later in hospitalization; N/A: not available; IAP: intra-abdominal pressure
in mm Hg
4
4 47% N/A N/A 1 3
4
11 67% N/A > 30 5 7
3 87% 1/3 45 3 0
9 59% 7/9 34 9 0
10 71% N/A 40 6 4
3 60% 2/3 52 3 0
7 47% 28% 37 7 0
10 57% 60% 23 10 0
in 16 patients at 8 hours, it actually increased by 47% in the remaining 15 patients. The
patients that were successfully managed with a lower rate of IV fluid resuscitation had less
severe injuries with a mean area of full-thickness burn of only 3%, while the remaining patients
had full-thickness burns covering 14% of their TBSA. The groups were otherwise very similar.
The mean 24 hour fluid resuscitation volume in the group where the rate was decreased was
5.6 mL/kg/%TBSA and was 7.7 mL/kg/%TBSA in the other group. The implication of this
study is that a 70 kg patient with a 50% TBSA burn with more than 15% of the TBSA burn
being full-thickness will receive approximately 27 liters over the first 24 hours even in the
absence of an inhalation injury.
A survey conducted by Engrav et al reviewed data on 50 patients and reported that 58%
received more than the 4.3 mL/kg/% TBSA compared with the 12% incidence reported by
13
Baxter.
These studies corroborate the suspicion of Dr Pruitt and others that we are significantly more aggressive with our fluid resuscitation than in years past. This increase in the
volume of fluid resuscitation probably does contribute to the relatively high incidence of IAH
and ACS in burn patients.
Balogh and colleagues from Houston have demonstrated that an aggressive fluid resuscita-
tion increases the risk of IAH and ACS in other populations of critically injured patients as
14
well.
They compared the outcomes from a standardized trauma resuscitation protocol using
a target of DO
I > 500 mL/min/m2 instead of a target of >600 mL/min/m2. The authors
2
found that the lower target required significantly less fluid and halved the incidence of IAH
(20% vs. 42%) and the incidence of ACS (8% vs. 16%). A separate study by that group retrospectively analyzed data from 188 patients who developed ACS over a 44 month period.
Their multiple logistic regression analysis linked the development of secondary ACS to the
volume of crystalloid infused, an average of over 30 liters in the first 24 hours in that population, a number that is in relatively close agreement with the multiple burn series mentioned
above.
15
Summary
Large volume fluid resuscitations required for patients with major burns place them at
significant risk of developing intra-abdominal hypertension. Patients who develop IAH or
ACS generally have TBSA burns of approximately 50% or more and often have a concurrent
inhalation injury
burn of 75% (Table 2), and more than half of the burn patients who develop ACS have
4-10
(Table 1). The subgroup of patients that develop ACS have a mean TBSA
185Secondary Abdominal Compartment Syndrome in Burns
Table 2. Characteristics of patients with burns and ACS
Series # pts TBSA Burn Inhalation IAP Survival
9
Latenser
8
Hobson
7
Corcos
5
Ivy
6
Ivy
Total 22 75% 8/12 41 6/22 (27%)
# pts: number of patients; TBSA: % Total body surface area burned; Inhalation: presence of inhalation
injury; IAP: mean intra-abdominal pressure of patients in that series; Survival: survival to discharge
from hospital; IAP: intra-abdominal pressure in mm Hg
4 83% 4/4 34 0/4
10 71% N/A 40 4/10
3 60% 2/3 52 1/3
3 87% 1/3 45 0/3
2 80% 1/2 40 1/2
sustained an inhalation injury.
talloid resuscitation utilizing protocols has been shown to drop the risk of IAH and ACS by
14
50%.
Hopefully, the incidence of IAH and ACS in patients with large burns can also be
5-9
In the general trauma population, less aggressive use of crys-
decreased by a resuscitation that utilizes a very tightly titrated fluid resuscitation protocol in
order to maintain a urine output greater than 0.5 mL/kg/h but less than 1 mL/kg/h. This
hypothesis can only be evaluated by a prospective trial performed collaboratively by multiple
burn centers.
An aggressive approach to IAH and ACS emphasizing early diagnosis and treatment may be
of benefit to some burn patients, but this has not been clearly demonstrated by a randomized
clinical trial. A variety of techniques have been used to decrease IAP in patients with IAH
including sedation, use of paralytic agents, diuresis, abdominal wall escharotomy and percutaneous catheter drainage of intraperitoneal fluid.
increased risk of mortality in patients who develop IAH, most patients with IAH do not go
onto develop full-blown ACS.
4-10
Some patients with ACS seem to benefit from percutaneous
catheter decompression, but often patients with ACS will require decompressive laparotomy.
Burn patients with ACS universally benefit from decompression during the initial postoperative period.
ACS do not survive to discharge.
4-6,8,9
Unfortunately, most burn patients who require decompressive laparotomy for
4-6,8,9
4-10
While several studies have documented an
4,9
The overall rate of survival to discharge in the burn
literature is only 29% (5/17) but this is substantially better than the expected survival rate of
0% (Table 3).
Table 3. Outcome of laparotomy for ACS
Series LAP Survival
Greenhalgh case series
5
Ivy
6
Ivy
9
Latenser
8
Hobson
Total 17 5 (29%)
LAP: number of patients undergoing decompressive laparotomy for ACS; Survival: number of patients
surviving to discharge
4
21
10
21
40
83
186
Abdominal Compartment Syndrome
Commentary
Andrew Kirkpatrick
Tremendous progress has been made in the last century in treating the most seriously burned
and injured. This progress has often been necessitated by both human conflict and recognition
of previously unknown complications unmasked by prior advances. The first world war in the
first half of this century led to the discovery that shock resulted from intravascular volume
deficits and that colloid and blood should be administered preoperatively.
of the last century, the frequent complication of early renal failure was all but eliminated through
the administration of aggressive crystalloid fluid resuscitation in burns and serious injury. Volumes administered sometimes seemed enormous (especially burns with inhalation injury).
Unfortunately, this practice was followed by the acute respiratory distress syndrome as a major
cause of morbidity and mortality in the third quarter.
5
Dedicated trauma care in the last quarter has led to efficient trauma systems providing early hemorrhage control, often entailing
damage control surgery to reduce exsanguinating deaths. This has also been followed by
multi-disciplinary care to alleviate single system organ failure, with multi-system organ failure
becoming a leading cause of in-hospital trauma death.
6
The last few years of the 20th century
have now seen a description of another post-injury complication that is also likely related to
treatment of hemorrhagic shock and severe burns. This is the secondary abdominal compartment syndrome (SACS). It is likely that this syndrome, closely associated and potentially bridging
shock and multi-system organ failure, is related to our current resuscitation practices. How we
resuscitate shock (either traumatic or burn-related), as well as how quickly the underlying
insult is addressed, may be important in the pathophysiology of the SACS.
Dr Balogh et al, from the University of Texas have published more than anyone else on the
SACS, and the world literature on this subject is thus greatly influenced by their thinking.
They have described the syndrome as an elusive, but very early complication of severe trauma
and resuscitation.
7
While pressure thresholds and definitions are controversial, they recognize
intra-abdominal pressures greater than 25 mm Hg accompanied by cardiac, respiratory, and
renal function as being diagnostic. They refer to SACS when there are no intraperitoneal inju-
ries, and specifically consider pelvic fracture related intraperitoneal hematomas without intraperitoneal injury to be secondary,
7,8
in consensus with other authors.
point as this particular injury comprises 73% of the SACS group. As other authors have considered SACS to apply only to those without injury or disease in the abdominopelvicregion,
this distinction should be noted. As almost half of this patient group required urgent angiographic
embolization for hemorrhage control in the Texas experience, they exemplify the presumed risk
factors for secondary ACS; namely delay in hemorrhage control temporized by with massive
crystalloid resuscitation in a prolonged pre-intensive care unit course.
been recognized to occur earlier in the hospital admission and unfortunately earlier decompression does not appear to improve outcome in this select minority of injured patients.
Dr. Ivy has concisely reviewed the limited literature describing the epidemiology and therapeutic implications of ACS occurring in setting of major burn injury, a literature which also
bears tribute to his personal work. He has also introduced the concept that clinicians may be
potentially harming their patients through over-vigorous fluid resuscitation. Sicker patients
with larger burns are now surviving, and these patients, with body surface area burns > 70%
and often with an associated inhalation injury are at great risk of developing the abdominal
compartment syndrome.
majority of ACS seen in the setting of major burns is not associated with primary abdominal
pathology or even abdominal wall eschar.
and it typically occurs either in response to our therapy, that being massive crystalloid infusion,
or as a result of a septic complication.
12,13
While combined abdominal injury is always a concern, the vast
12-14
ACS in this setting has been termed secondary,
14
Factors relating to the required fluid volume are burn
surface area, depth of the burn, presence of inhalation injury, which are fixed, and the indiscriminate use of fluid boluses and timing of resuscitation which are clinician-dependant.
1-3
In the second half
9,10
This is an important
8
Secondary ACS has
7,11
4
11
187Secondary Abdominal Compartment Syndrome in Burns
Linear regression predicts elevated intra-abdominal pressure to 25 mm Hg, a level that usually
requires intervention,
15
after 250 mL/kg or a burn injury of 63% BSA according to the Parkland
resuscitation formula. This syndrome has been variably described by various authors but essentially reflects clinically evident end-organ dysfunction on the basis of acute and sustained raised
intra-abdominal pressures.
affect the course of critically injured patients through impaired visceral perfusion, and potentiation of multi-organ dysfunction, even if the full-blown syndrome is not evident.
16,17
It also likely that raised intra-abdominal pressures also adversely
18,19
When
the SACS does develop, it typically has a dramatic response to decompressive laparotomy,
although the presence of SACS after burn injury has ominous implications for hospital discharge (29% survivors).
Fluid resuscitation has been defined as a treatment regimen involving fluid replacement
intended to minimize the effects of (hemorrhagic) shock and to stabilize the hemodynamic
response.
cially to the penumbra of injury. In contradistinction to previous generations who may have
under-resuscitated patients though, we appear to have entered an era of “fluid creep”,
2
The goal being to maintain perfusion to each and every cell of the organism, espe-
20,21
with
crystalloid fluids administered in excess of that required, so that perfusion and oxygen delivery
are not increased, but are actually paradoxically decreased due to the detrimental systemic
effects of SACS.
22,23
Precedent has shown that identified limitations and problems that were previously obscured
by conditions now successfully treated, quickly become topics for new research problems; hopefully the SACS will be as well.
4
Many anti-inflammatory approaches have been or are being
investigated to ameliorate the primary insult, including hypertonic saline resuscitative strategies. Closed loop computer-driven resuscitation using fluid administration proportional to the
measured value of a predefined end-point may achieve favorable outcomes with less over-all
fluid administration and avoidance of over-resuscitation,
end-point is still critical in avoiding over-resuscitation and the ACS.
24
although choosing the appropriate
22
Until novel approaches
are proven though, due diligence will be required of all clinicians to avoid all possible delay in
hemorrhage control and to optimize the fluid resuscitation to the best of their abilities, implying a continued presence at the foot of the bed.
Commentary References
1. Cannon WB. Traumatic shock. New York: D Appelton Co, 1923.
2. Introduction. Pope A, French G, Longnecker DE, eds. Fluid Resuscitation: State of the Science for
Treating Combat Casualties and Civilian Injuries. Washington, DC: National Academy Press,
1999:9-18.
3. Pruitt BA, Pruitt JH, Davis JH. History. Moore EE, Feliciano DV, Mattox KL, eds. Trauma. 5th
ed. New York: McGraw-Hill, 2004:3-19.
4. Pruitt BA. The development of the International Society for Burn Injuries and progress in burn
care: the whole is greater than the sum of its parts. Burns 1999; 25:683-96.
5. Moore FA, McKinley BA, Moore EE. The next generation in shock resuscitation. Lancet 2004;
363:1988-96.
6. Sauaia A, Moore FA, Moore EE et al. Epidemiology of trauma death: a reassessment. J Trauma
1995; 38:185-93.
7. Balogh Z, McKinley BA, Cocanour CS et al. Secondary abdominal compartment syndrome is an
elusive early complication of traumatic shock resuscitation. Am J Surg 2002; 184:538-44.
8. Balogh Z, McKinley BA, Holcomb JB et al. Both primary and secondary abdominal compartment
syndrome can be predicted early and are harbringers of multiple organ failure. J Trauma 2003;
54:848-61.
9. Maxwell RA, Fabian T, Croce M et al. Secondary abdominal compartment syndrome: an
underappreciated manifestation of severe hemorrhagic shock. J Trauma 1999; 47:995-9.
10. Kopelman T, Harris C, Miller R et al. Abdominal compartment syndrome in patients with isolated extraperitoneal injuries. J Trauma 2000; 49:744-9.
11. Biffl WL, Moore EE, Burch JM et al. Secondary abdominal compartment syndrome is a highly
lethal event. Am J Surg 2001; 182:645-8.
12. Ivy ME, Possenti PP, Kepros J et al. Abdominal compartment syndrome in patients with burns. J
Burn Care Rehabil 1999; 20:351-3.
188
13. Ivy ME, Atweh NA, Palmer J et al. Intra-abdominal hypertension and abdominal compartment
syndrome in burn patients. J Trauma 2000; 49:387-91.
14. Hobson KG, Young KM, Ciraulo A et al. Release of abdominal compatment syndrome improves
survival in patients with burn injury. J Trauma 2002; 53:1129-34.
15. Nathens AB, Brenneman FD, Boulanger BR. The abdominal compartment syndrome. Can J Surg
1997; 40:254-8.
16. Schein M, Wittman DH, Aprahamian CC et al. The abdominal compartment syndrome: the
physiolgical and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg 1995;
180:745-52.
17. Kirkpatrick AW, Brenneman FD, McLean RF et al. Is clinical examination an accurate indicator
of raised intra-abdominal pressure in critically injured patients. Can J Surg 2000; 43:207-11.
18. Ivatury RR, Porter JM, Simon RJ et al. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH
and abdominal compartment syndrome. J Trauma 1998; 44:1016-23.
19. Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and bacterial translocation in the
abdominal compartment syndrome. J Trauma 1997; 43:852-5.
20. Engrav LH, Colescott PL, Kemalyan N et al. A biopsy of the use of the Baxter formula to resuscitate burns or do we do it like Charlie did it? J Burn Care Rehabil 2000; 21:91-5.
21. Pruitt BA. Protection from excessive resuscitation: “Pushing the pendulum back”. J Trauma 2000;
49:567-8.
22. Balogh Z, McKinley BA, Cocanour CS et al. Supranormal trauma resuscitation causes more cases
of abdominal compartment syndrome. Arch Surg 2003; 138:637-43.
23. Balogh Z, MooreFA, McKinley BA. Supranormal trauma resuscitation and abdominal compartment syndrome: In reply [letter]. Arch Surg 2004; 139:226-7.
24. Chaisson NF, Kirschner RA, Deyo DJ et al. Near-infrared spectroscopy-guided closed-loop resuscitation of hemorrhage. J Trauma 2003; 54:S183-S192.
Abdominal Compartment Syndrome
References
1. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a criterion for
abdominal reexploration. Ann Surg 1984; 199:28-30.
2. Burrows R, Edington J, Robbs JV. A wolf in wolf’s clothing-the abdominal compartment syndrome. S Afr Med J 1995; 85:46-48.
3. Maxwell RA, Fabian TC, Croce MA et al. Secondary abdominal compartment syndrome: An
underappreciated manifestation of severe hemorrhagic shock. J Trauma 1999; 47:995-999.
4. Greenhalgh DG, Warden GD. The importance of intra-abdominal pressures measurements in burned
children. J Trauma 1994; 36:685-690.
5. Ivy ME, Possenti PP, Kepros J et al. Abdominal compartment syndrome in patients with burns. J
Burn Care Rehabil 1999; 20:351-353.
6. Ivy ME, Atweh NA, Palmer J et al. Intra-abdominal hypertension and abdominal compartment
syndrome in burn patients. J Trauma 2000; 49:387-391.
7. Corcos AC, Sherman HF. Percutaneous treatment of secondary abdominal compartment syndrome.
J Trauma 2001; 51:1062-1064.
8. Hobson KG, Young KM, Ciraulo A et al. Release of abdominal compartment syndrome improves
survival in patients with burn injury. J Trauma 2002; 53:1129-1134.
9. Latenser BA, Kowal-Vern A, Kimball D et al. A pilot study comparing percutaneous decompression with decompressive laparotomy for acute abdominal compartment syndrome in thermal injury. J Burn Care Rehabil 2002; 23:190-195.
10. Tsoutsos D, Rodopoulou S, Keramidas E et al. Early escharotomy as a measure to reduce
intra-abdominal hypertension in full-thickness burns of the thoracic and abdominal area. World J
Surg 2003; 27:1323-1328.
11. Pruitt BA. Protection from excessive resuscitation:”Pushing the pendulum back”. J Trauma 2000;
49:567-568.
12. Cartotto RC, Innes M, Musgrave MA et al. How well does the parkland formula estimate actual
fluid resuscitation volumes? J Burn Care Rehabil 2002; 23:258-265.
13. Engrav LH, Colescott PL, Kemalyan N et al. A biopsy of the use of the Baxter formula to resuscitate burns or do we do it like Charlie did it? J Burn Care Rehabil 2000; 21:91-95.
14. Balogh Z, McKinley BA, Cocanour CS et al. Supra-normal trauma resuscitation causes more cases
of abdominal compartment syndrome. Arch Surg 2003; 138:637-643.
15. Balogh Z, Mckinley BA, Holcomb JB et al. Both primary and secondary abdominal compartment
syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma 2003;
54:848-861.
CHAPTER 15
Morbid Obesity and Chronic
Intra-Abdominal Hypertension
Giselle G. Hamad* and Andrew B. Peitzman
Abstract
orbid obesity has achieved epidemic proportions in the United States. A vast number of comorbid conditions are associated with morbid obesity, including metabolic
M
hyperlipidemia. An association between obesity and intra-abdominal hypertension has been
demonstrated, which explains the predisposition to pseudotumor cerebri, hypertension, pulmonary disorders, stress urinary incontinence, gastroesophageal reflux, and incisional hernia in
morbid obesity. Weight loss results in a reduction in intra-abdominal pressure and resolution
of comorbidities.
Morbid Obesity and Weight-Related Comorbidities
percent of American adults are overweight and 31 percent are obese.
obesity-attributable medical expenditures reached $75 billion per year in 2003.
duces a multitude of chronic illnesses affecting virtually every organ system (Table 1). These
weight-related comorbidities account for the heightened mortality among the morbidly obese.
Central obesity has been linked to an elevation in intra-abdominal pressure (IAP), creating a
chronic intra-abdominal compartment syndrome.
the metabolic syndrome, whose major components include insulin resistance, hypertension,
and hyperlipidemia. Intra-abdominal fat is independently associated with all five criteria that
comprise the metabolic syndrome.
found that waist circumference, which reflects central obesity, was a significant predictor of
comorbidity while body mass index (BMI), which is defined as body weight divided by the
height squared (kg/m
tient to cardiovascular disease. The etiology of metabolic syndrome remains unclear and the
pathophysiologic mechanisms underlying the comorbid illnesses are controversial.
is elevated in obesity.
and examined their association with weight-related comorbidities.
urinary bladder pressures in 84 morbidly obese patients prior to performing gastric bypass and
compared them to measurements in five nonobese subjects. Sagittal abdominal diameters were
recorded by measurement of the apex of the abdominal girth with the patient supine. Obese
patients had significantly higher bladder pressures than the nonobese. Urinary bladder pressure
syndrome, which consists of central obesity, insulin resistance, hypertension, and
Morbid obesity has achieved epidemic proportions in the United States. An estimated 66
Two types of obesity have been described: peripheral, or gynecoid, and central, or android.
3
Central obesity is one of the hallmarks of
4
In a study of over 14,000 subjects, Janssen and colleagues
2
), was not.5 The components of metabolic syndrome predispose a pa-
A number of studies have shown that urinary bladder pressure, which is a surrogate for IAP,
6-9
Sugerman et al demonstrated the relationship between obesity and IAP
1
In the United States,
6
The investigators measured
2
Obesity in-
*Corresponding Author: Giselle G. Hamad—Department of Surgery, University of Pittsburgh
Medical Center, Pittsburgh, Pennsylvania, U.S.A. Email: hamadg@upmc.edu.
Abdominal Compartment Syndrome, edited by Rao R. Ivatury, Michael L. Cheatham,
Manu L. N. G. Malbrain and Michael Sugrue. ©2006 Landes Bioscience.
190
Table 1. Obesity-related comorbidities
Neurologic Hypercoagulable states
Migraine headaches Deep venous thrombosis
Pseudotumor cerebri Venous stasis disease
Respiratory
Obstructive sleep apnea
Asthma Stress incontinence
Obesity hypoventilation syndrome Renal insufficiency
Cardiovascular Reproductive
Hypertension Amenorrhea
Hyperlipidemia Dysmenorrhea
Congestive heart failure Polycystic ovary syndrome
Coronary artery disease
Left ventricular hypertrophy Degenerative joint disease
Metabolic syndrome Gout
Varicose veins Incisional hernia
Venous stasis disease
Gastrointestinal
Gastroesophageal reflux Anxiety
Cholelithiasis
Nonalcoholic steatohepatitis Colorectal
Endocrine
Type II diabetes mellitus
Hypothyroidism
Abdominal Compartment Syndrome
Pulmonary embolism
Genitourinary
Connective tissue
Psychiatric
Depression
Malignancies
Endometrial
correlated significantly with sagittal abdominal diameter (r = 0.6, r2 = 0.36, p < 0.0001). In
obese patients with intra-abdominal pressure-related comorbidities, including obesity
hypoventilation, gastroesophageal reflux, venous stasis, stress incontinence, and incisional hernia, bladder pressures were significantly elevated compared to obese patients without
pressure-related comorbidity (19 ± 0.8 vs 15 ± 1.3, P < 0.05). The data suggest that central
obesity elevates IAP, which then induces the comorbidities related to IAH.
Additional studies have demonstrated the relationship between elevated IAP and obesity. A
significant correlation between IAP and BMI has been demonstrated.
7,8
IAP, measured
transvaginally, transrectally, or transvesically, correlated strongly with BMI, with a correlation
coefficient of 0.76 (p<0.0001) with transrectal measurements and a correlation coefficient of
0.71 (p<0.0001) for bladder pressures. McIntosh et al measured IAP during pressure flow
studies in 100 consecutive men and demonstrated a correlation coefficient of 0.52 between
BMI and IAP.
9
Weight loss results in a reduction in IAP. In a prospective study of obese patients undergoing gastric bypass, significant reductions in sagittal abdominal diameter (32 ± 1 to 20 ± 2 cm,
p<0.001) and bladder pressure (17 ± 2 to 10 ± 1 cm H
following gastric bypass.
10
Patients lost 69 ± 4% of excess body weight. A decrease in the
O, p < 0.001) were observed one year
2
number of weight-related comorbidities per patient was also observed after gastric bypass (2.9
± 0.4 to 1 ± 0.2). These data illustrate the relationship between obesity, abdominal pressure,
and weight-related comorbidities.
Hemodynamic Alterations in Obesity
The deleterious effect of intra-abdominal hypertension (IAH) on the cardiovascular system
has been evaluated in large animal models. Intra-abdominal hypertension creates reproducible
disturbances in the hemodynamic system. An increase in IAP produces hypertension in a
191Morbid Obesity and Chronic Intra-Abdominal Hypertension
canine model.11 An intraperitoneal balloon was progressively inflated weekly over four weeks
to a pressure of 25 mm Hg above baseline, maintained at that pressure for two weeks, and then
deflated over two weeks. With balloon inflation, systolic and diastolic blood pressure increased
compared to controls, and returned to baseline with decompression. In a swine model using an
intra-abdominal balloon, elevations in IAP caused a reduction in cardiac index and systemic
vascular resistance index and an increase in central venous pressure and cardiac filling pres-
12
sures.
In central obesity, intra-abdominal hypertension results from an excess of intra-abdominal
fat, which has been found to promote hypertension. In a study of obese women by Kanai et al,
the amount of intra-abdominal fat was determined by calculating the ratio of the area of
intra-abdominal visceral fat to subcutaneous fat by CT scan.
13
The authors found a correlation
between intra-abdominal fat accumulation and hypertension. Compared to obese normotensive subjects, the obese hypertensive subjects had a significantly higher proportion of
intra-abdominal visceral fat. The authors suggested that intra-abdominal fat accumulation may
contribute to the pathogenesis of hypertension in obesity. Hayashi et al studied 563
Japanese-American subjects and measured intra-abdominal fat area by CT.
14
Intra-abdominal
fat area was found to be a significant predictor of hypertension.
Data suggest that weight loss improves blood pressure by decreasing intra-abdominal fat.
Kanai et al reported on the effect of diet-induced weight loss on blood pressure.
15
Obese hypertensive women were placed on a 12-week hypocaloric diet. The ratio of visceral to subcutaneous fat was significantly reduced with weight loss. Mean blood pressure fell from 112 +/- 9 to
101 +/- 12 mm Hg (p < .001). The change in mean blood pressure after weight loss did not
correlate with the change in body weight or BMI, but did correlate with the reduction in
visceral fat or ratio of visceral fat to subcutaneous fat. The authors concluded that in obese
hypertensive subjects, a decrease in intra-abdominal fat, rather than simply body weight, reduced blood pressure.
The derangements in hemodynamic parameters in the morbidly obese are more pronounced
with laparoscopic surgery as a result of the carbon dioxide pneumoperitoneum. A significant
elevation in systolic blood pressure accompanied pneumoperitoneum in obese patients relative
to controls, whose systolic pressure did not rise significantly.
16
Left ventricular wall stress was
higher in obese patients at baseline and significantly increased with pneumoperitoneum. Therefore, obese patients are more susceptible to a compromise in myocardial oxygenation with
pneumoperitoneum.
Whether the pathogenesis of hypertension is related to the mechanical pressure of visceral
fat on the cardiovascular system leading to an activation of the renin-angiotension-aldosterone
system, or it is the result of proinflammatory mediators released by the adipose tissue is unclear.
Pseudotumor Cerebri
Elevated IAP is associated with pseudotumor cerebri (PTC), or idiopathic intracranial hypertension, a condition that is most frequently seen in obese females. Clinical manifestations
include debilitating headache, dizziness, nausea, vomiting, pulsatile tinnitus, and papilledema.
Intracranial hypertension is present without evidence of hydrocephalus, mass lesion, structural, or vascular lesion. Sugerman and colleagues hypothesized that PTC is secondary to IAH.
They found that bladder pressure and sagittal abdominal diameter were significantly elevated
in patients with elevated intracranial pressure compared with nonobese controls. The
transesophageal pleural pressure, central venous pressure, mean pulmonary artery pressure,
and pulmonary artery occlusion pressure were markedly higher than in obese patients without
PTC. The data suggest that central obesity raises IAP with resultant increases in pleural pressure and cardiac filling pressure. Venous return from the brain is therefore impaired, leading to
the increased intracranial pressure associated with PTC.
An additional study by Sugerman et al further supports the hypothesis that IAH causes
PTC in obesity.
18
Seven morbidly obese women with PTC were treated with a negative
17
192
Abdominal Compartment Syndrome
Table 2. Initial effect of ABSHELL™ on symptoms of pseudotumor cerebri in morbid
obesity
Headache Tinnitus
Before ABSHELL™ 6.8 ± 0.8 4.2 ± 0.5
5 min after ABSHELL™ 4.2 ± 0.8* 1.8 ± 0.5**
1 h after ABSHELL™ 2.2 ± 0.8† 1.7 ± 0.5
* p < 0.05; ** p < 0.02; †p < 0.01. Reprinted with permission from: Sugerman HJ et al. Int J Obes Relat
Metab Disord 2001; 25:486-90. ©2001 Nature Publishing Group.
†
abdominal pressure device designed to alleviate the effects of IAH. The device consisted of a
fiberglass shell that was applied to the abdomen, vacuum tubing, and two vacuum pumps.
Headache and pulsatile tinnitus resolved within five minutes (Table 2); relief lasted as long as
the patients wore the devices. Symptoms gradually returned once the devices were removed.
Patients who wore the device as they slept awoke without headache or tinnitus.
For more durable control of symptoms, surgically induced weight loss may reduce symptoms of PTC. Sugerman and colleagues demonstrated a reduction in headache and tinnitus in
18 out of 19 patients with PTC within four months of bariatric surgery.
19
Intra-abdominal hypertension causes disturbances in cranial hemodynamics. Bloomfield et
al reported significant increases in intracranial pressure and pleural pressure in a swine model
of abdominal hypertension, while cerebral perfusion pressure decreased significantly.
12
The
data suggest that an elevation in intra-abdominal pressure causes a rise in intrathoracic pressure, which induces an increase in intracranial pressure and a decrease in cerebral perfusion
pressure.
Pulmonary Abnormalities and Obesity
The morbidly obese suffer from a higher risk of pulmonary complications. This may be
explained by the adverse effects of IAH on the mechanical properties of the respiratory system
and pulmonary hemodynamics in association with obesity. In the previously described
intra-abdominal balloon experiment in swine by Bloomfield et al, significant increases in pleural pressure and pulmonary artery occlusion pressure were associated with IAH.
ings are in concordance with the abnormalities seen clinically in morbidly obese patients with
obesity hypoventilation syndrome (OHS), which is defined as an arterial oxygen tension ≤ 55
mg Hg and/or arterial carbon dioxide tension ≥ 47 mm Hg.
Obesity has adverse mechanical effects on the pulmonary system. Pelosi et al measured
bladder pressure and pulmonary mechanics in 8 nonsmoking obese subjects
these with data from a study of 16 nonobese subjects by D’Angelo et al.
Functional residual capacity was lower in the obese subjects, while IAP was higher. Airway
resistance and the alveolar-arterial oxygenation gradient were higher in the obese subjects. The
data suggest that the unopposed elevation in abdominal pressure contributes to the reduction
in lung volume and hypoxemia seen in obesity.
Intra-abdominal hypertension causes disturbances in pulmonary hemodynamics. Sugerman
performed pulmonary artery catheterization in 46 morbidly obese patients, 26 with and 20
without OHS.
22
Mean pulmonary artery pressure and mean pulmonary artery occlusion pressures were significantly higher in the OHS patients compared to those without OHS. Despite
mechanical ventilation and correction of hypoxemia and hypercarbia, which would reduce the
effect of hypoxic pulmonary artery vasoconstriction, cardiac filling pressures remained elevated.
Following surgically induced weight loss, pressures normalized.
20
and compared
21
12
These find-
193Morbid Obesity and Chronic Intra-Abdominal Hypertension
Gastroesophageal Reflux
Gastroesophageal reflux disease (GERD) and hiatal hernia are prevalent among the morbidly obese. Factors that promote GERD include a short intra-abdominal lower esophageal
sphincter (LES), reduced LES pressure, elevated intra-abdominal pressure, abnormal esophageal clearance, and impaired gastric emptying. The IAH associated with obesity alters the
pressure gradient between the stomach and the gastroesophageal junction,
placement of the LES above the diaphragm. A sliding hiatal hernia results, which promotes
25
GERD.
prior to undergoing gastric bypass, hiatal hernia was present in 52.6% and reflux esophagitis
was diagnosed in 31.4%.
In a study of 345 patients with morbid obesity who underwent evaluation for GERD
26
Twenty-four pH monitoring was abnormal in 73%. Ruhl and
Everhart published the results of the National Health and Nutrition Examination Survey
(NHANES I), in which approximately 12,000 patients were followed for a median of 18.5
27
years.
The data suggested that hospitalization for reflux was associated with a 5kg/m2 incre-
ment in BMI.
Obese patients undergoing traditional antireflux operations have a higher recurrence rate
than normal weight or overweight patients. Patients with documented GERD who had failed
medical management were classified into groups based on their BMI: normal, overweight, and
28
obese.
Following laparoscopic Nissen fundoplication or Belsey Mark IV, 31.3% of the obese
patients had recurrent reflux, while only 4.5% of the normal group (p < 0.0001 vs obese) and
8% of the overweight group (p = 0.001 vs obese) recurred. The authors suggested that the
increase in IAP in obesity contributes to the failure of antireflux surgery by loosening the crural
repair and fundoplication.
In light of the failure of traditional antireflux surgery in obesity, Roux-en-Y gastric bypass
has been recommended for treatment of GERD in this population.
banded gastroplasty is not only unsuccessful at controlling GERD,
33
reflux.
23,24
leading to dis-
29,30
In contrast, vertical
31,32
but also exacerbates
Genitourinary System
The pathogenesis of hypertension and renal dysfunction in obesity may be explained by
IAH. In a porcine model, elevated IAP caused an elevation in renal venous pressure with a
concomitant reduction of urine output, an increase in plasma renin and an increase in aldoster-
34
one.
Therefore, sodium and water are retained and vasoconstriction occurs. Furthermore,
glomerulopathy and proteinuria may result from the increase in renal venous pressure.
Obesity is associated with stress urinary incontinence (SUI).
from coughing or sneezing lead to involuntary leakage of urine. Bai et al compared 98 women
with SUI and 102 control women without SUI.
36
The BMI in the SUI group was significantly
35
Abrupt increases in IAP
higher compared to controls, but there was no correlation between BMI and urodynamic parameters. In Noblett’s study of BMI and IAP, 48% had genuine stress urinary incontinence and
13% had severe prolapse.
37
The authors suggested that the etiology of stress urinary incontinence might be explained by the chronic elevation of IAP in obesity, which exerts stress on the
pelvic floor.
Massive weight loss may result in an improvement in lower urinary tract function. Bump et
al demonstrated a significant improvement in both objective and subjective measures of stress
urinary incontinence following surgically-induced weight loss.
38
Only three of 12 patients
with SUI prior to bariatric surgery complained of incontinence postoperatively. A significant
reduction was seen in vesical pressure, the change in bladder pressure with coughing, the number of incontinence episodes, and the need for absorptive pads.
Incisional Hernias
Chronic intra-abdominal hypertension has been postulated to be a cause of incisional hernia in obesity. Sugerman et al published the results of a study comparing the incidence of
incisional hernia following open gastric bypass for morbid obesity versus total colectomy with
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